NFIB facilitates replication licensing by acting as a genome organizer

Wenting Zhang, Yue Wang, Yongjie Liu, Cuifang Liu, Yizhou Wang, Lin He, Xiao Cheng, Yani Peng, Lu Xia, Xiaodi Wu, Jiajing Wu, Yu Zhang, Luyang Sun, Ping Chen, Guohong Li, Qiang Tu, Jing Liang () and Yongfeng Shang ()
Additional contact information
Wenting Zhang: Peking University Health Science Center
Yue Wang: Peking University Health Science Center
Yongjie Liu: University of Chinese Academy of Sciences
Cuifang Liu: Chinese Academy of Sciences
Yizhou Wang: Chinese Academy of Sciences
Lin He: Peking University Health Science Center
Xiao Cheng: Peking University Health Science Center
Yani Peng: Peking University Health Science Center
Lu Xia: Peking University Health Science Center
Xiaodi Wu: Capital Medical University
Jiajing Wu: Capital Medical University
Yu Zhang: Peking University Health Science Center
Luyang Sun: Peking University Health Science Center
Ping Chen: Capital Medical University
Guohong Li: Chinese Academy of Sciences
Qiang Tu: University of Chinese Academy of Sciences
Jing Liang: Peking University Health Science Center
Yongfeng Shang: Peking University Health Science Center

Nature Communications, 2023, vol. 14, issue 1, 1-22

Abstract: Abstract The chromatin-based rule governing the selection and activation of replication origins in metazoans remains to be investigated. Here we report that NFIB, a member of Nuclear Factor I (NFI) family that was initially purified in host cells to promote adenoviral DNA replication but has since mainly been investigated in transcription regulation, is physically associated with the pre-replication complex (pre-RC) in mammalian cells. Genomic analyses reveal that NFIB facilitates the assembly of the pre-RC by increasing chromatin accessibility. Nucleosome binding and single-molecule magnetic tweezers shows that NFIB binds to and opens up nucleosomes. Transmission electron microscopy indicates that NFIB promotes nucleosome eviction on parental chromatin. NFIB deficiency leads to alterations of chromosome contacts/compartments in both G1 and S phase and affects the firing of a subset of origins at early-replication domains. Significantly, cancer-associated NFIB overexpression provokes gene duplication and genomic alterations recapitulating the genetic aberrance in clinical breast cancer and empowering cancer cells to dynamically evolve growth advantage and drug resistance. Together, these results point a role for NFIB in facilitating replication licensing by acting as a genome organizer, shedding new lights on the biological function of NFIB and on the replication origin selection in eukaryotes.

Date: 2023
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DOI: 10.1038/s41467-023-40846-1

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